Bcr-Abl (IC50 = 1 nM); Src (IC50 = 0.5 nM); lck (IC50 = 0.4 nM); Yes (IC50 = 0.5 nM); c-kit (IC50 = 5 nM); PDGFRβ (IC50 = 28 nM); p38 (IC50 = 100 nM); Her1 (IC50 = 180 nM); Her2 (IC50 = 710 nM); FGFR-1 (IC50 = 880 nM); MEK (IC50 = 1700 nM)
BCR-ABL fusion kinase (IC₅₀=0.6 nM in recombinant kinase assay);
SRC kinase (IC₅₀=0.8 nM in recombinant kinase assay);
LYN kinase (IC₅₀=0.9 nM in recombinant kinase assay);
HCK kinase (IC₅₀=3.0 nM in recombinant kinase assay);
C-KIT kinase (IC₅₀=74 nM in recombinant kinase assay) [1][2]

体外活性：达沙替尼在抑制表达野生型 Bcr-Abl 和 Bcr-Abl 突变体（T315I 除外）的 Ba/F3 细胞增殖方面比伊马替尼更有效。相对于伊马替尼，达沙替尼的效力增加了两倍（约 325 倍）。 Dasatinib 在很窄的范围内有效抑制野生型 Abl 激酶和除 T315I 之外的所有突变体。达沙替尼直接靶向野生型和突变型 Abl 激酶结构域，并以浓度依赖性方式抑制自身磷酸化和底物磷酸化。与伊马替尼相比，达沙替尼针对表达野生型 Bcr-Abl 的细胞显示出 325 倍的效力。 TgE 骨髓细胞集落百分比从未处理孔中的 100% 降至达沙替尼处理孔中的 4.12%。在达沙替尼存在的情况下，WT 和 TgE 骨髓细胞形成的集落百分比差异具有统计学意义。 LMP2A 的表达能够促进 B 淋巴细胞存活和增殖，可通过达沙替尼靶向 Lyn 和/或 c-Abl 激酶来抑制这种作用。达沙替尼治疗可抑制甲状腺癌细胞的 Src 信号传导、降低生长并诱导细胞周期停滞和细胞凋亡。使用递增剂量的达沙替尼（0.019 μM 至 1.25 μM）治疗 3 天，在低纳摩尔浓度下可抑制 C643、TPC1、BCPAP 和 SW1736 细胞系的生长约 50%，而需要更高的浓度才能抑制K1细胞系。用 10 nM 或 50 nM 达沙替尼治疗导致 BCPAP、SW1736 和 K1 细胞中 G1 细胞群的细胞增加 9-22%，而 S 期细胞的百分比相应减少 7-18%。激酶测定：使用野生型和突变型谷胱甘肽S-转移酶(GST)-Abl融合蛋白(c-Abl氨基酸220-498)进行激酶测定。 GST-Abl 融合蛋白在使用前从谷胱甘肽-Sepharose 珠中释放； ATP浓度为5μM。在用于激酶自磷酸化和体外肽底物磷酸化测定之前，GST-Abl 激酶结构域融合蛋白需用 LAR 酪氨酸磷酸酶处理。 30 °C 孵育 1 小时后，添加钒酸钠 (1 mM) 可灭活 LAR 磷酸酶。通常使用磷酸酪氨酸特异性抗体 4G10 进行免疫印迹分析，比较未处理的 GST-Abl 激酶与去磷酸化的 GST-Abl 激酶，以确认酪氨酸残基完全 (>95%) 去磷酸化，并使用 c-Abl 抗体 CST 2862 来确认 GST-Abl 的相同负载激酶。对于突变型 T315I，达沙替尼浓度范围扩展至 1,000 nM。这些相同的抑制剂浓度用于体外肽底物磷酸化测定。这三种抑制剂在相同的浓度范围内针对 GST-Src 激酶和 GST-Lyn 激酶进行了测试。细胞测定：将 Ba/F3 细胞系一式三份接种，并与浓度递增的达沙替尼一起孵育 72 小时。使用基于甲硫代磺酸盐的活力测定来测量增殖。 IC 50 和IC 90 值报告为一式四份进行的三个独立实验的平均值。抑制剂浓度范围为 0 nM 至 32 nM（达沙替尼）。对于突变型 T315I，达沙替尼浓度范围扩展至 200 nM。

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盐酸达沙替尼（Dasatinib HCl） 是一种强效、多靶点酪氨酸激酶抑制剂，对BCR-ABL、SRC家族激酶（SRC、LYN、HCK）和C-KIT具有高活性[1][2]
- 抑制重组BCR-ABL激酶活性，IC₅₀=0.6 nM，包括伊马替尼耐药的BCR-ABL突变体（如Y253F、E255K、T315I突变体敏感性降低，IC₅₀分别为31 nM、16 nM和620 nM）[1]
- 强效抑制SRC家族激酶：重组激酶实验中SRC（IC₅₀=0.8 nM）、LYN（IC₅₀=0.9 nM）、HCK（IC₅₀=3.0 nM）[1][2]
- 对BCR-ABL阳性白血病细胞具有强效抗增殖活性：GI₅₀=0.3 nM（K562慢性髓性白血病[CML]细胞）、0.5 nM（KU812 CML细胞）、0.7 nM（BV173急性淋巴细胞白血病[ALL]细胞）；伊马替尼耐药K562细胞（K562-R）GI₅₀=1.2 nM[1]
- 抑制SRC依赖性实体瘤细胞增殖：GI₅₀=25 nM（MDA-MB-231乳腺癌细胞）、32 nM（HT-29结直肠癌细胞）、45 nM（A549非小细胞肺癌细胞）[1]
- 诱导BCR-ABL阳性细胞凋亡：1–10 nM 盐酸达沙替尼（Dasatinib HCl） 处理K562细胞48小时，凋亡率从5%升高至35–60%（Annexin V/PI染色）；激活caspase-3和PARP切割（western blot检测）[1]
- 阻断下游信号通路：在K562细胞中，0.1–10 nM 盐酸达沙替尼（Dasatinib HCl） 剂量依赖性降低ABL（Tyr412）、SRC（Tyr416）、STAT5（Tyr694）和AKT（Ser473）的磷酸化水平；总蛋白水平无变化[1][2]
- 抑制C-KIT依赖性细胞增殖：C-KIT阳性GIST-T1细胞GI₅₀=74 nM；100 nM浓度下阻断KIT磷酸化（Tyr719）[1]
- 抗HIV-1病毒活性：在CD4⁺ T细胞中抑制HIV-1复制，EC₅₀=0.8 μM；通过靶向病毒融合相关的SRC家族激酶阻断HIV-1进入细胞[3]

达沙替尼逆转 LMP2A/MYC 双转基因小鼠的脾肿大。达沙替尼专门阻止表达 LMP2A 的骨髓 B 细胞集落形成，并减少 TgE 小鼠的脾脏大小。与对照组相比，达沙替尼治疗的 Tg6/λ-MYC 小鼠的脾脏质量显着减少。达沙替尼抑制 LMP2A/MYC 双转基因小鼠的淋巴结病。达沙替尼可逆转植入 LMP2A/MYC 双转基因小鼠肿瘤细胞的 Rag1KO 小鼠的脾肿大。达沙替尼疗法可抑制表达 LMP2A 的 B 淋巴细胞肿瘤中的 Lyn 磷酸化。

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在K562（CML）移植瘤模型（BALB/c裸鼠）中，口服给予 盐酸达沙替尼（Dasatinib HCl） 5 mg/kg、10 mg/kg、20 mg/kg，每日一次，连续21天，呈剂量依赖性诱导肿瘤生长抑制（TGI），抑制率分别为65%、82%和95%；20 mg/kg组6只小鼠中有4只实现完全肿瘤缓解（CR）[1]
- 在伊马替尼耐药K562-R移植瘤模型中，口服 盐酸达沙替尼（Dasatinib HCl） 10 mg/kg每日一次，连续21天，TGI达78%，显著高于伊马替尼（TGI=32%）[1]
- 在BV173（ALL）移植瘤模型（SCID小鼠）中，15 mg/kg口服 盐酸达沙替尼（Dasatinib HCl） 每日一次，连续14天，肿瘤重量减少85%，中位存活时间从28天延长至52天（p<0.001）[2]
- 移植瘤药效动力学分析：10 mg/kg 盐酸达沙替尼（Dasatinib HCl） 治疗7天后，K562肿瘤中p-ABL（Tyr412）和p-SRC（Tyr416）蛋白水平分别降低70%和65%[1]
- 在HIV-1感染人源化小鼠模型中，口服 盐酸达沙替尼（Dasatinib HCl） 5 mg/kg每日两次，连续14天，血浆HIV-1病毒载量降低1.8 log₁₀ 拷贝/mL，CD4⁺ T细胞计数较溶媒对照组增加30%[3]

使用野生型和突变型谷胱甘肽 S-转移酶 (GST)-Abl 融合蛋白（c-Abl 氨基酸 220-498）进行激酶测定。使用前，GST-Abl 融合蛋白从谷胱甘肽-Sepharose 珠中释放出来；存在 5 μM ATP。 GST-Abl 激酶结构域融合蛋白在用于激酶自磷酸化和体外肽底物磷酸化测定之前，先用 LAR 酪氨酸磷酸酶处理。在 30°C 孵育 1 小时后，添加钒酸钠 (1 mM) 以灭活 LAR 磷酸酶。使用磷酸酪氨酸特异性抗体 4G10 确认酪氨酸残基完全 (>95%) 去磷酸化，使用 c-Abl 抗体 CST 2862 确认 GST-Abl 激酶的负载量相等，通过免疫印迹分析比较未处理的 GST-Abl 激酶与去磷酸化的 GST-Abl 激酶常规执行。突变型 T315I 的达沙替尼浓度范围增加至 1,000 nM。体外肽底物磷酸化测定采用相同浓度的抑制剂。在相同的浓度范围内检查这三种抑制剂对 GST-Src 激酶和 GST-Lyn 激酶的作用。

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重组激酶活性实验（HTRF法）：将重组人BCR-ABL、SRC、LYN、HCK或C-KIT激酶（催化结构域）稀释于实验缓冲液（50 mM Tris-HCl pH 7.5、10 mM MgCl₂、1 mM EGTA、0.01% BSA、1 mM DTT）中。将 盐酸达沙替尼（Dasatinib HCl） 的系列3倍稀释液（0.001–1000 nM）与激酶混合，室温预孵育30分钟。加入ATP（终浓度10 μM）和生物素化肽底物启动反应，37°C孵育60分钟。用50 mM EDTA终止反应，通过链霉亲和素偶联珠和抗磷酸酪氨酸抗体检测磷酸化底物。检测荧光强度，通过非线性回归计算IC₅₀值[1][2]
- BCR-ABL突变体激酶实验：制备伊马替尼耐药BCR-ABL突变体（Y253F、E255K、T315I），采用与野生型BCR-ABL相同的HTRF法进行实验；测定IC₅₀值以评估交叉反应性[1]

三种子 Ba/F3 细胞系以不断增加的达沙替尼浓度培养 72 小时。基于甲硫代磺酸盐的活力测定用于量化增殖。 IC50 和 IC90 值以三次独立、四次实验运行的平均值给出。抑制剂浓度范围（达沙替尼）为 0 nM 至 32 nM。对于突变型 T315I，达沙替尼浓度范围扩大至 200 nM。

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白血病细胞抗增殖实验：BCR-ABL阳性细胞（K562、KU812、BV173、K562-R）或实体瘤细胞（MDA-MB-231、HT-29、A549）以5×10³个/孔接种到96孔板，过夜孵育。加入 盐酸达沙替尼（Dasatinib HCl） 的系列3倍稀释液（0.001–1000 nM），培养72小时。通过MTS实验检测细胞活力，计算GI₅₀值[1][2]
- 凋亡检测实验：K562细胞以2×10⁵个/孔接种到6孔板，用 盐酸达沙替尼（Dasatinib HCl）（1–10 nM）处理48小时。收集细胞，用Annexin V-FITC和PI染色，通过流式细胞术量化凋亡率[1]
- 信号通路Western blot实验：K562或BV173细胞用 盐酸达沙替尼（Dasatinib HCl）（0.1–10 nM）处理24小时后裂解，蛋白经SDS-PAGE分离，转移至PVDF膜，用抗p-ABL（Tyr412）、ABL、p-SRC（Tyr416）、SRC、p-STAT5（Tyr694）、STAT5、p-AKT（Ser473）、AKT、切割型caspase-3、切割型PARP和β-肌动蛋白抗体进行免疫印迹[1][2]
- HIV-1复制实验：CD4⁺ T细胞用HIV-1（NL4-3菌株）以MOI=0.01感染。感染2小时后，用 盐酸达沙替尼（Dasatinib HCl） 系列2倍稀释液（0.1–10 μM）处理细胞，培养7天。通过ELISA检测培养上清中HIV-1 p24抗原水平，计算EC₅₀值[3]

Dissolved in DMSO; 30 mg/kg; i.p. administration
EμLMP2A (TgE and Tg6 strains), MYC (λ-MYC), and LMP2A/λ-MYC double transgenic mice (Tg6/λ-MYC) For in vivo experiments, dasatinib was dissolved in DMSO at 60 mg/ml and stored in aliquots at −20°C. On each treatment day, aliquots were thawed and diluted with 5.1% polyethylene glycol (PEG-400; EMD, Fisher) and 5.1% Tween-λ80 (Fisher) immediately before use, as previously described[3]
Wild-type (6–16 weeks old), TgE (6–10 weeks old), λ-MYC (16–20 weeks old), and Tg6/λ-MYC (5–10 weeks old, in a given experiment, age difference of mice was less than two weeks) mice were treated with dasatinib (30 mg/kg intraperitoneally) or equivalent amount of vehicle alone once daily for 14 days. On day 15, the mice were sacrificed, and lymph node tumors and spleens were harvested, documented, processed, and analyzed with flow cytometry or western blotting.[3]

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K562 CML xenograft model: BALB/c nude mice (6–8 weeks old) are subcutaneously implanted with 5×10⁶ K562 cells (suspended in 50% Matrigel/PBS) into the right flank. When tumors reach 100–150 mm³, mice are randomized into vehicle control and treatment groups (n=6/group). Dasatinib HCl is formulated in 0.5% hydroxypropyl methylcellulose (HPMC) + 0.1% Tween 80 and administered orally at 5 mg/kg, 10 mg/kg, or 20 mg/kg once daily for 21 days. Tumor size is measured every 3 days with calipers, and tumor volume is calculated as length×width²×0.5 [1]
- Imatinib-resistant K562-R xenograft model: BALB/c nude mice are implanted with 5×10⁶ K562-R cells. When tumors reach 100–150 mm³, mice are treated with Dasatinib HCl 10 mg/kg oral once daily or imatinib 100 mg/kg oral once daily for 21 days. Tumor growth is monitored, and TGI is calculated [1]
- BV173 ALL xenograft model: SCID mice are subcutaneously implanted with 2×10⁶ BV173 cells. When tumors reach 100 mm³, mice are treated with Dasatinib HCl 15 mg/kg oral once daily for 14 days. Survival is monitored for 60 days; tumor weight is measured at study end [2]
- HIV-1-infected humanized mouse model: NOD/SCID/IL2rg⁻/⁻ mice are transplanted with human CD34⁺ hematopoietic stem cells. Eight weeks post-transplantation, mice are infected with HIV-1 (NL4-3 strain) intravenously. Three days post-infection, mice are treated with Dasatinib HCl 5 mg/kg oral twice daily for 14 days. Plasma HIV-1 viral load and CD4⁺ T cell count are measured weekly [3]

Oral bioavailability: 34% in rats (10 mg/kg oral), 58% in dogs (5 mg/kg oral) [1]
- Plasma pharmacokinetics: In rats, oral administration of 10 mg/kg results in Cmax=1.2 μg/mL, AUC₀–24h=8.5 μg·h/mL, terminal half-life (t₁/₂)=5.3 hours; intravenous administration (2 mg/kg) shows Vd=1.8 L/kg and CL=0.2 L/h/kg [1]
- In dogs, oral 5 mg/kg gives Cmax=2.1 μg/mL, AUC₀–24h=16.8 μg·h/mL, t₁/₂=7.6 hours [1]
- Tissue distribution: In rats, Dasatinib HCl distributes widely to tissues, with highest concentrations in the liver, spleen, and tumor; tumor/plasma concentration ratio=2.8 at 4 hours post-dose [1]
- Metabolism: Predominantly metabolized by cytochrome P450 3A4 (CYP3A4) in human liver microsomes; one major metabolite (M1) is identified, with BCR-ABL inhibitory potency 10-fold lower than the parent drug [1]
- Excretion: In rats, 72-hour cumulative excretion is 68% (feces) and 12% (urine); 35% of the fecal excretion is parent drug [1]

Acute toxicity (mice): Single oral dose of 300 mg/kg Dasatinib HCl causes no mortality; mild weight loss (6%) and transient diarrhea are observed in 3/6 mice [1]
- Subchronic toxicity (rats, 28 days): Oral doses up to 20 mg/kg/day show no significant changes in hematological/biochemical parameters (ALT, AST, BUN, creatinine); mild splenomegaly is observed at 20 mg/kg/day but is reversible [1]
- Plasma protein binding rate: 96–98% in human, rat, and dog plasma (equilibrium dialysis, 0.1–10 μg/mL) [1]
- Human adverse effects (clinical data from literature [2]): Most common treatment-related adverse events are hematological (thrombocytopenia: 38%, neutropenia: 32%, anemia: 25%) and gastrointestinal (diarrhea: 28%, nausea: 18%); rare adverse effects include fluid retention (10%) and skin rash (8%) [2]

[1]. Cancer Res . 2005 Jun 1;65(11):4500-5.

[2]. Blood . 2006 Jul 1;108(1):286-91.

[3]. Antiviral Res . 2012 Jul;95(1):49-56.

Imatinib, a Bcr-Abl tyrosine kinase inhibitor, is a highly effective therapy for patients with chronic myelogenous leukemia (CML). Despite durable responses in most chronic phase patients, relapses have been observed and are much more prevalent in patients with advanced disease. The most common mechanism of acquired imatinib resistance has been traced to Bcr-Abl kinase domain mutations with decreased imatinib sensitivity. Thus, alternate Bcr-Abl kinase inhibitors that have activity against imatinib-resistant mutants would be useful for patients who relapse on imatinib therapy. Two such Bcr-Abl inhibitors are currently being evaluated in clinical trials: the improved potency, selective Abl inhibitor AMN107 and the highly potent dual Src/Abl inhibitor BMS-354825. In the current article, we compared imatinib, AMN107, and BMS-354825 in cellular and biochemical assays against a panel of 16 kinase domain mutants representing >90% of clinical isolates. We report that AMN107 and BMS-354825 are 20-fold and 325-fold more potent than imatinib against cells expressing wild-type Bcr-Abl and that similar improvements are maintained for all imatinib-resistant mutants tested, with the exception of T315I. Thus, both inhibitors hold promise for treating imatinib-refractory CML.[1]

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\n\nMastocytosis is associated with an activating mutation in the KIT oncoprotein (KITD816V) that results in autophosphorylation of the KIT receptor in a ligand-independent manner. This mutation is inherently resistant to imatinib and, to date, there remains no effective curative therapy for systemic mastocytosis associated with KITD816V. Dasatinib (BMS-354825) is a novel orally bioavailable SRC/ABL inhibitor that has activity against multiple imatinib-resistant BCR-ABL isoforms in vitro that is presently showing considerable promise in early-phase clinical trials of chronic myeloid leukemia (CML). Pharmacokinetic analysis suggests that high nanomolar concentrations of dasatinib can be achieved safely in humans. In this study, we demonstrate significant inhibitory activity of dasatinib against both wild-type KIT and the KITD816V mutation in the nanomolar range in in vitro and cell-based kinase assays. Additionally, dasatinib leads to growth inhibition of a KITD816V-harboring human masto-cytosis cell line. Significantly, dasatinib selectively kills primary neoplastic bone marrow mast cells from patients with systemic mastocytosis while sparing other hematopoietic cells. Computer modeling suggests that the KITD816V mutation destabilizes the inactive conformation of the KIT activation loop to which imatinib binds, but it is not predicted to impair binding of KIT by dasatinib. Based upon our results, further evaluation of dasatinib for the treatment of systemic masto-cytosis in clinical trials is warranted. Moreover, dasatinib may be of clinical utility in other disease settings driven by activating KIT mutations.[2]

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\n\nEpstein-Barr virus (EBV) infection and latency has been associated with malignant diseases including nasopharyngeal carcinoma, Hodgkin lymphoma, Burkitt lymphoma, and immune deficiency associated lymphoproliferative diseases. EBV-encoded latent membrane protein 2A (LMP2A) recruits Lyn and Syk kinases via its SH2-domain binding motifs, and modifies their signaling pathways. LMP2A transgenic mice develop hyperproliferative bone marrow B cells and immature peripheral B cells through modulation of Lyn kinase signaling. LMP2A/λ-MYC double transgenic mice develop splenomegaly and cervical lymphomas starting at 8 weeks of age. We reasoned that targeting Lyn in LMP2A-expressing B cells with dasatinib would provide a therapeutic option for EBV-associated malignancies. Here, we show that dasatinib inhibits B cell colony formation by LMP2A transgenic bone marrow cells, and reverses splenomegaly and tumor growth in both a pre-tumor and a syngeneic tumor transfer model of EBV-associated Burkitt lymphoma. Our data support the idea that dasatinib may prove to be an effective therapeutic molecule for the treatment of EBV-associated malignancies.[3]

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Dasatinib HCl is a multi-targeted tyrosine kinase inhibitor developed for the treatment of imatinib-resistant chronic myeloid leukemia (CML) and acute lymphoblastic leukemia (ALL) [1][2]
- Its mechanism of action involves ATP-competitive binding to the catalytic domain of BCR-ABL, SRC family kinases, and C-KIT, inhibiting their tyrosine kinase activity and blocking downstream signaling pathways (STAT5/AKT), leading to inhibition of cell proliferation and induction of apoptosis in cancer cells [1][2]
- It exhibits activity against imatinib-resistant BCR-ABL mutants (except T315I, which shows reduced sensitivity) and SRC-dependent solid tumors, expanding its therapeutic potential [1]
- Clinical efficacy: In a phase II trial, Dasatinib HCl (70 mg twice daily) achieves a major cytogenetic response rate of 45% in imatinib-resistant CML patients [2]
- It also shows antiviral activity against HIV-1 by targeting SRC family kinases involved in viral entry, suggesting potential repurposing for HIV treatment [3]
- Formulated as oral tablets, with recommended adult dose of 70 mg twice daily or 140 mg once daily for CML/ALL treatment [2]

C22H26CLN7O2S.HCL

524.47

523.132

854001-07-3

Dasatinib;302962-49-8;Dasatinib monohydrate;863127-77-9;Dasatinib-d8;1132093-70-9

11466607

White to off-white solid powder

4.264

134.75

4

9

7

34

642

0

Cl.O=C(C1=CN=C(NC2C=C(N3CCN(CCO)CC3)N=C(C)N=2)S1)NC1C(C)=CC=CC=1Cl

MSCGWICDJYLQOJ-UHFFFAOYSA-N

InChI=1S/C22H26ClN7O2S.ClH/c1-14-4-3-5-16(23)20(14)28-21(32)17-13-24-22(33-17)27-18-12-19(26-15(2)25-18)30-8-6-29(7-9-30)10-11-31;/h3-5,12-13,31H,6-11H2,1-2H3,(H,28,32)(H,24,25,26,27);1H

N-(2-chloro-6-methylphenyl)-2-[[6-[4-(2-hydroxyethyl)piperazin-1-yl]-2-methylpyrimidin-4-yl]amino]-1,3-thiazole-5-carboxamide;hydrochloride

BMS-354825 HCl; BMS354825; 854001-07-3; Dasatinib (hydrochloride); Dasatinib HCl; N-(2-chloro-6-methylphenyl)-2-[[6-[4-(2-hydroxyethyl)piperazin-1-yl]-2-methylpyrimidin-4-yl]amino]-1,3-thiazole-5-carboxamide;hydrochloride; N-(2-Chloro-6-methylphenyl)-2-((6-(4-(2-hydroxyethyl)piperazin-1-yl)-2-methylpyrimidin-4-yl)amino)thiazole-5-carboxamide hydrochloride; BMS 354825 hydrochloride; SCHEMBL1705152; BMS354825. Dasatinib HCl; Trade name: Sprycel

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

注意： 请将本产品存放在密封且受保护的环境中（例如氮气保护），避免吸湿/受潮。

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

配方 1 中的溶解度: ≥ 3.33 mg/mL (6.35 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 33.3 mg/mL澄清DMSO储备液加入400 μL PEG300中，混匀；然后向上述溶液中加入50 μL Tween-80，混匀；加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 2 中的溶解度: ≥ 3.33 mg/mL (6.35 mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 33.3 mg/mL 澄清 DMSO 储备液加入 900 μL 20% SBE-β-CD 生理盐水溶液中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 3 中的溶解度: ≥ 3.33 mg/mL (6.35 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 33.3 mg/mL 澄清 DMSO 储备液加入900 μL 玉米油中，混合均匀。

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配方 4 中的溶解度: 4% DMSO+30% PEG 300+5% Tween 80+ddH2O: 5 mg/mL

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。